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Topic starter
28/10/2019 3:12 pm
Lipids. 2007 Apr;42(4):297-305.
Leucine and calcium regulate fat metabolism and energy partitioning in murine adipocytes and muscle cells.
Sun X, Zemel MB.
Department of Nutrition, University of Tennessee, 1215 W. Cumberland Avenue, Knoxville, TN 37996-1920, USA.
Dietary calcium modulation of adiposity is mediated, in part, by suppression of calcitriol, while the additional effect of dairy products is mediated by additional components; these include the high concentration of leucine, a key factor in the regulation of muscle protein turnover. We investigated the effect of leucine, calcitriol and calcium on energy metabolism in murine adipocytes and muscle cells and on energy partitioning between adipocytes and skeletal muscle. Leucine induced a marked increase in fatty acid oxidation in C2C12 muscle cells (P<0.001) and decreased FAS expression by 66% (P<0.001) in 3t3-L1 adipocytes. Calcitriol decreased muscle cell fatty acid oxidation by 37% (P<0.001) and increased adipocyte FAS gene expression by threefold (P<0.05); these effects were partially reversed by either leucine or calcium channel antagonism with nifedipine. Co-culture of muscle cells with adipocytes or incubation with 48-h adipocyte conditioned medium decreased muscle fatty acid oxidation by 62% (P<0.001), but treating adipocytes with leucine and/or nifedipine attenuated this effect. Leucine, nifedipine and calcitriol also modulated adiponectin production and thereby exerted additional indirect effects on fatty acid oxidation in C2C12 myotubes. Adiponectin increased IL-15 and IL-6 release by myotubes and partially reversed the inhibitory effects of calcitriol. Comparable effects of leucine, calcitriol and adiponectin were found in myotubes treated with conditioned medium derived from adipocytes or co-cultured with adipocytes. These data suggest that leucine and nifedipine promote energy partitioning from adipocytes to muscle cells, resulting in decreased energy storage in adipocytes and increasing fatty acid utilization in muscle.
dr frankenstein
28/10/2019 3:42 pm
care to make a conclusion in plain english cause I have no id what all of this is supposed to mean...
Topic starter
28/10/2019 4:10 pm
Re: Leucine, great stuff.
care to make a conclusion in plain english cause I have no id what all of this is supposed to mean...
leucine increase fat oxidation,adipocytes are fat cells.
fat from adipose tissue go to the muscle for being burned.
These data suggest that leucine and nifedipine promote energy partitioning from adipocytes to muscle cells, resulting in decreased energy storage in adipocytes and increasing fatty acid utilization in muscle.
dr frankenstein
28/10/2019 4:39 pm
Re: Re: Leucine, great stuff.
leucine increase fat oxidation,adipocytes are fat cells.
fat from adipose tissue go to the muscle for being burned.
Nice find. Nice translation.
Thanks!
28/10/2019 4:56 pm
to say nothing of the fact that leucine is the "meat and potatoes" amino acid in BCAAs and significantly contribute to protein synthesis if taken before and after workouts.
jb
28/10/2019 5:23 pm
Good study. I have a hard time interpreting the numbers. How much of a difference in fat oxidation did the study find when leucine was administered (and how much leucine)?
Also, is there a conclusion to be drawn about using dairy products or calcium supplements?
28/10/2019 5:40 pm
Hm... I wonder how long it will be before a supplement co comes out with an esterfied or hcl version. It's pretty cool that BCAA's are an old school idea and science is proving it true.
Seabiscuit Hogg is a fictious internet character. It is not recommended that you receive medical advice from fictious internet characters.
SBH :)
Topic starter
28/10/2019 6:07 pm
Diabetes. 2007 Jun;56(6):1647-54.
Increasing dietary leucine intake reduces diet-induced obesity and improves glucose and cholesterol metabolism in mice via multimechanisms.
Zhang Y, Guo K, LeBlanc RE, Loh D, Schwartz GJ, Yu YH.
Department of Pediatrics, Division of Molecular Genetics, Columbia University, New York, NY 10032, USA.
Leucine, as an essential amino acid and activator of mTOR (mammalian target of rapamycin), promotes protein synthesis and suppresses protein catabolism. However, the effect of leucine on overall glucose and energy metabolism remains unclear, and whether leucine has beneficial effects as a long-term dietary supplement has not been examined. In the present study, we doubled dietary leucine intake via leucine-containing drinking water in mice with free excess to either a rodent chow or a high-fat diet (HFD). While it produced no major metabolic effects in chow-fed mice, increasing leucine intake resulted in up to 32% reduction of weight gain (P < 0.05) and a 25% decrease in adiposity (P < 0.01) in HFD-fed mice. The reduction of adiposity resulted from increased resting energy expenditure associated with increased expression of uncoupling protein 3 in brown and white adipose tissues and in skeletal muscle, while food intake was not decreased. Increasing leucine intake also prevented HFD-induced hyperglycemia, which was associated with improved insulin sensitivity, decreased plasma concentrations of glucagon and glucogenic amino acids, and downregulation of hepatic glucose-6-phosphatase. Additionally, plasma levels of total and LDL cholesterol were decreased by 27% (P < 0.001) and 53% (P < 0.001), respectively, in leucine supplemented HFD-fed mice compared with the control mice fed the same diet. The reduction in cholesterol levels was largely independent of leucine-induced changes in adiposity. In conclusion, increases in dietary leucine intake substantially decrease diet-induced obesity, hyperglycemia, and hypercholesterolemia in mice with ad libitum consumption of HFD likely via multiple mechanisms.
dr frankenstein
28/10/2019 6:37 pm
this is really good stuff and leucine is very inexpensive.
jb
28/10/2019 7:04 pm
Congrats Oswaldo for the find and for the good explanation, I think that bro ought to be a little bit more polite .
"The medals don't mean anything and the glory doesn't last. It's all about your happiness. The rewards are going to come, but my happiness is just loving the sport and having fun performing" ~ Jackie Joyner Kersee.
Topic starter
28/10/2019 7:22 pm
Congrats Oswaldo for the find and for the good explanation, I think that bro ought to be a little bit more polite .
just lazyness gui.............
and remember, english is not my native language.......if not....
dr frankenstein
28/10/2019 7:45 pm
Hm... I wonder how long it will be before a supplement co comes out with an esterfied or hcl version. It's pretty cool that BCAA's are an old school idea and science is proving it true.
You can get esterfied BCAA's now.
What does Leucine taste like?
BCAA are pretty bad, I'd be happy to add in some more Leucine, but not if it the cause of the bad taste.
28/10/2019 8:01 pm
the leucine i get from BAC does not taste that bad but i am able to gulp down some pretty bad stuff!
jb
Topic starter
28/10/2019 8:21 pm
Cell Metabolism, Vol 6, 181-194, 05 September 2007.
Disruption of BCATm in Mice Leads to Increased Energy Expenditure Associated with the Activation of a Futile Protein Turnover Cycle.
Pengxiang She, Tanya M. Reid, Sarah K. Bronson, Thomas C. Vary, Andras Hajnal, Christopher J. Lynch, and Susan M. Hutson.
Leucine is recognized as a nutrient signal; however, the long-term in vivo consequences of leucine signaling and the role of branched-chain amino acid (BCAA) metabolism in this signaling remain unclear. To investigate these questions, we disrupted the BCATm gene, which encodes the enzyme catalyzing the first step in peripheral BCAA metabolism. BCATm−/− mice exhibited elevated plasma BCAAs and decreased adiposity and body weight, despite eating more food, along with increased energy expenditure, remarkable improvements in glucose and insulin tolerance, and protection from diet-induced obesity. The increased energy expenditure did not seem to be due to altered locomotor activity, uncoupling proteins, sympathetic activity, or thyroid hormones but was strongly associated with food consumption and an active futile cycle of increased protein degradation and synthesis. These observations suggest that elevated BCAAs and/or loss of BCAA catabolism in peripheral tissues play an important role in regulating insulin sensitivity and energy expenditure.
http://download.cellmetabolism.org/...13107002252.pdf
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Cell Metabolism, Vol 6, 155-156, 05 September 2007.
Leucing Weight with a Futile Cycle.
Susan K. Fried1, and Malcolm Watford.
The essential amino acid leucine serves as a signal that activates protein synthesis.
http://www.cellmetabolism.org/conte...550413107002318
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"This could conceivably be done in humans not by turning off a gene, but by designing a drug to block the enzyme that breaks down leucine. In theory, people on such a drug could eat a normal diet and still shed pounds, although what the side effects might be is unknown. Fried, who co-authors a piece in Cell Metabolism describing the new work, says that any such therapy is "a long way down the road". It is good to be cautious, she says, when tinkering with something as fundamental as protein synthesis."
http://www.nature.com/news/2007/070...l/070903-4.html
.
dr frankenstein
28/10/2019 8:51 pm
or perhaps by increasing the dose of the leucine.
jb